Combined Curcumin and G-CSF Therapy Attenuates Cisplatin-Induced Leukopenia and Hepatotoxicity in an Experimental Murine Model
Keywords:
Cisplatin toxicity, Curcumin; Granulocyte Colony-Stimulating Factor, chemotherapy-induced leukopenia, drug-induced hepatotoxicity, oxidative stressAbstract
Despite the potent efficacy of Cisplatin in combating various solid malignancies, its therapeutic utility is often compromised by severe toxic manifestations. Notable clinical constraints include the induction of systemic leukopenia and significant hepatic impairment. The objective of this investigation was to evaluate the potential of a co-administration strategy involving Curcumin and Granulocyte Colony-Stimulating Factor (G-CSF) in providing synergistic cytoprotection against the aforementioned toxicological challenges within a murine experimental framework. A cohort of fifty male albino mice was utilized, following a randomized allocation into five experimental clusters. These included a baseline Control, a group challenged with Cisplatin (7.5 mg/kg, i.p.), and treatment cohorts receiving either Curcumin (200 mg/kg, p.o.), G-CSF (30 μg/kg, s.c.), or a synergistic integration of both agents (Cis+Cur+G-CSF). Therapeutic efficacy was evaluated through hematological profiling, assessment of hepatic functional enzymes (ALT, AST and ALP), and measurement of oxidative stress biomarkers (MDA, SOD and GSH). Cisplatin administration produced marked leukopenia accompanied by significant hepatic oxidative injury. Although treatment with either Curcumin or G-CSF alone conferred partial improvement, the combined regimen produced the most pronounced protective response, with the greatest restoration of WBC counts (p < 0.001) and substantial normalization of liver biochemical indices. The evidence presented suggests that the dual administration of Curcumin and G-CSF offers a potential pharmacological paradigm for mitigating the toxic sequelae inherent to platinum-derived chemotherapeutics.

